scholarly journals Alterations in basal and glucose-stimulated voltage-dependent Ca2+ channel activities in pancreatic beta cells of non-insulin-dependent diabetes mellitus GK rats.

1996 ◽  
Vol 97 (11) ◽  
pp. 2417-2425 ◽  
Author(s):  
S Kato ◽  
H Ishida ◽  
Y Tsuura ◽  
K Tsuji ◽  
M Nishimura ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
Insulin Dependent Diabetes Mellitus ◽  
Insulin Dependent Diabetes ◽  
Dependent Diabetes Mellitus ◽  
Gk Rats ◽  
Voltage Dependent ◽  
Insulin Dependent

scholarly journals Endogenous secretion of insulin and its relationship with immunogenetic markers in infants with insulin-dependent diabetes mellitus

1995 ◽  
Vol 41 (1) ◽  
pp. 4-6
Author(s):  
I. V. Osokina ◽  
L. N. Scherbacheva ◽  
N. B. Lebedev ◽  
I. M. Belovalova ◽  
A. P. Knyazeva ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
High Risk ◽  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
Insulin Dependent Diabetes Mellitus ◽  
Insulin Dependent Diabetes ◽  
Dependent Diabetes Mellitus ◽  
C Peptide ◽  
Insulin Dependent ◽  
Hla Phenotype

The level of C-peptide is a marker determining the clinical course of insulin-dependent diabetes mellitus (IDDM). The factors influencing the volume of residual endogenous secretion of insulin in IDDM patients are not yet well known. In order to elucidate the effect of HLA-phenotype on the residual function .of pancreatic beta-cells and the course of diabetes, 114 children, 55 boys and 59 girls aged 8 months to 6.5 years, suffering from IDDM, were examined. HLA phenotype was detected by the standard microlymphocytotoxic test. Fifty-nine HLA antigens of classes I and II, locuses A, B, DR, DQ were taken into consideration. Basal and radial C-peptide was assessed by radioimmunoassay. The pancreatic insulin-secretory function was found reduced in young patients with IDDM. The mean values of C- peptide were 0.13 ± 0.01 nmol/liter. Residual secretion of insulin was revealed in 56.2% of children. HLA markers of high risk of IDDM development in the first yeais of life were revealed: DQw3. DR3/4. DR4, DR3, B8 antigens. The markers of high risk of diabetes DR3 and DR4, and moreover, DR3/4. as well as the age by the disease onset and duration of IDDM were found to influence the size and duration of functioning of beta-cells.

Endogenous secretion of insulin and its relationship with immunogenetic markers in infants with insulin-dependent diabetes mellitus

1995 ◽  
Vol 41 (1) ◽  
pp. 4-6
Author(s):  
I. V. Osokina ◽  
L. N. Scherbacheva ◽  
N. B. Lebedev ◽  
I. M. Belovalova ◽  
A. P. Knyazeva ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
High Risk ◽  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
Insulin Dependent Diabetes Mellitus ◽  
Insulin Dependent Diabetes ◽  
Dependent Diabetes Mellitus ◽  
C Peptide ◽  
Insulin Dependent ◽  
Hla Phenotype

RESULTS:The level of C-peptide is a marker determining the clinical course of insulin-dependent diabetes mellitus (IDDM). The factors influencing the volume of residual endogenous secretion of insulin in IDDM patients are not yet well known. In order to elucidate the effect of HLA-phenotype on the residual function .of pancreatic beta-cells and the course of diabetes, 114 children, 55 boys and 59 girls aged 8 months to 6.5 years, suffering from IDDM, were examined. HLA phenotype was detected by the standard microlymphocytotoxic test. Fifty-nine HLA antigens of classes I and II, locuses A, B, DR, DQ were taken into consideration. Basal and radial C-peptide was assessed by radioimmunoassay. The pancreatic insulin-secretory function was found reduced in young patients with IDDM. The mean values of C- peptide were 0.13 ± 0.01 nmol/liter. Residual secretion of insulin was revealed in 56.2% of children. HLA markers of high risk of IDDM development in the first yeais of life were revealed: DQw3. DR3/4. DR4, DR3, B8 antigens. The markers of high risk of diabetes DR3 and DR4, and moreover, DR3/4. as well as the age by the disease onset and duration of IDDM were found to influence the size and duration of functioning of beta-cells.

scholarly journals Amylin under examination. Fibrillogenic potential of the troublesome molecule

2018 ◽  
Vol 72 ◽  
pp. 295-306
Author(s):  
Małgorzata Marszałek
Keyword(s):  
Diabetes Mellitus ◽  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
Cell Loss ◽  
Insulin Dependent Diabetes Mellitus ◽  
Dependent Diabetes Mellitus ◽  
Cell Dysfunction ◽  
Insulin Dependent ◽  
Methodological Difficulties

In patients or animals affected by 2 type diabetes mellitus (diabetes mellitus type 2 DM2, non-insulin dependent diabetes mellitus NIDDM) some pathological deposits, called amyloid are observed among cells of islets of Langerhans. Among others constituents deposits consist of insoluble, fibrillar form of polipeptide neurohormone called amylin, produced by pancreatic beta cells.. It is thought that formation of fibrillar deposits of misfolded and aggregated polipeptide is highly toxic to beta cells and leads to cell dysfunction, cell loss, pancreas destruction and progress of the disease. Due to the extreme insolubility of this polipeptide and its instant fibrillation amylin constitutes a methodological problem and there is a need for a special methodology in experiments. This article reviews the most important experiments aimed at discovering fibrillogenic potential of amylin and models of interaction of the polipeptide’s monomers in man and rat. Numerous methodological difficulties in amylin research has been also emphasized.

scholarly journals Immunotherapy for insulin-dependent diabetes mellitus

1995 ◽  
Vol 41 (4) ◽  
pp. 43-48
Author(s):  
I. I. Dedov ◽  
I. A. Abugova ◽  
M. Sh. Shamhalova ◽  
P. I. Shishko
Keyword(s):  
Diabetes Mellitus ◽  
Beta Cells ◽  
Interleukin 1 ◽  
Hla Antigens ◽  
Nod Mice ◽  
Insulin Dependent Diabetes Mellitus ◽  
Insulin Dependent Diabetes ◽  
Tnf Alpha ◽  
Dependent Diabetes Mellitus ◽  
Insulin Dependent

The autoimmune nature of insulin-dependent diabetes mellitus (IDDM) is currently undeniable. In the 80s, some features of its pathogenesis were determined: on beta cells of patients with newly diagnosed IDDM, overexpression of class I HLA antigens was detected; on beta and alpha cells of isolated islets of Langerhans, expression of class II HLA antigens in combination with tumor necrosis factor (TNF-alpha) and gamma-interferon (gamma-IF) was detected; the presence or absence of Asp-57 in the N-end of the beta1 domain of the HLADQ beta chain has been shown to be positively associated with IDDM in humans and NOD mice; it was revealed that macrophage interleukin-1 (IL-1) and TNF-alpha have a damaging effect on beta cells: IL-1 exhibits selective beta-cell cytotoxicity in low molar concentrations, and the effect of IL-1 is potentiated by TNF-alpha; it was determined that early infiltration during the development of inflammation of pancreas in BB rats is caused by macrophages and monocytes; destruction of beta cells is performed by T-helpers and natural killers. Thus, the autoimmune concept of the disease necessitates the use of immunotherapy to slow the development of IDDM.

Type I Insulin-Dependent Diabetes Mellitus: a Model for Autoimmune Polygenic Disorders

1996 ◽  
Vol 10 (1) ◽  
pp. 81-87 ◽  
Author(s):  
W.E. Winter
Keyword(s):  
Diabetes Mellitus ◽  
Pancreatic Beta Cells ◽  
Insulin Treatment ◽  
Premature Mortality ◽  
Insulin Dependent Diabetes Mellitus ◽  
Insulin Dependent Diabetes ◽  
Dependent Diabetes Mellitus ◽  
Acid Decarboxylase ◽  
Type I ◽  
Insulin Dependent

Insulin-dependent diabetes mellitus (IDD) affects between one in 250 and one in 500 Americans. The inheritance of IDD is non-Mendelian and polygenic. Genetic susceptibility predominantly results from specific alleles in the HLA complex and insulin gene region. Autoimmune destruction of pancreatic beta cells leads to profound insulinopenia (Atkinson and Maclaren, 1990). Without insulin treatment, fatal diabetic ketoacidosis results. Even with insulin treatment, after 10 to 20 years of IDD, devastating micro- and macrovascular complications lead to significant morbidity and premature mortality (Rosenbloom, 1983). In order to prevent this catastrophic disease and its consequences, we must understand the pathogenesis and immunogenetics of insulitis (the histologic lesion characteristic of IDD), whose ultimate expression is beta cell necrosis (Cudworth, 1978; Cahill and McDevitt, 1981; Eisenbarth, 1986). Current advances include recognition of new IDD-autoantigens (e.g., glutamic acid decarboxylase), susceptibility genes (e.g., HLA-DQB 1 *0201 and 0302), and the development of trials to prevent IDD through tolerization to IDD-autoantigens (e.g., insulin) (Maclaren, 1993; Winter et al., 1993). Unlocking the genetic mechanisms responsible for IDD can also reveal more general mechanisms involved in other organ-specific autoimmune diseases.

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